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Blood acidification by lactic acid infusion converts bicarbonate to CO 2 . This effect can be exploited to increase the transmembrane PCO 2  gradient of an extracorporeal membrane lung, resulting in a significant increase of extracorporeal CO 2  removal. Lactic acid, however, is an energetic substrate and its metabolism might increase total body CO 2  production (VCO 2 ), limiting the potential beneficial effects of this technique. The aim of our study was to compare VCO₂ during isocaloric infusion of lactic acid or glucose.    Methods  Six pigs (45 ± 5 kg) were sedated and mechanically ventilated. Estimated caloric needs were 2,300–2,400 Kcal/die (95 to 100 Kcal/h). A sequence of two steps lasting four hours each was performed: 1) Glucose, 97 kcal/h were administered as 50% glucose solution, and 2) Lactic Acid, approximately 48.5 kcal/h were administered as lactic acid and approximately 48.5 kcal/h as 50% glucose solution. This sequence was repeated three times with two-hour intervals. Every hour VCO₂, arterial blood gases and lactate were measured. Blood glucose level was kept constant by titrating an insulin infusion, ventilation was adjusted to maintain arterial PCO 2  at 50 mmHg, a normal value for our animal model.    Results  During Lactic Acid steps VCO 2  increased less than 5% compared to the Glucose steps (282 vs. 269 ml/min,  P  <0.05); blood glucose did not differ between the two groups (respectively 101 ± 12 vs. 103 ± 8 mg/dl). Arterial lactate was always lower than 3 mmol/L. Arterial pH was lower during Lactic Acid steps (7.422 vs. 7.445,  P  <0.05).    Conclusions  Replacing 50% of the caloric input with lactic acid increased total CO 2  production by less than 5% compared to an equal caloric load provided entirely by a 50% glucose solution.

critical care

Infusion of 2.5 meq/min of lactic acid minimally increases CO2 production compared to an isocaloric glucose infusion in healthy anesthetized, mechanically ventilated pigs